Creation Of Sah And Induction Of Vasospasm

Models of SAH should ideally consist of placement or injection of blood that surrounds a cerebral artery and results in consistent and reproducible, delayed vasospasm that lasts for several days, as confirmed by angiographic or morphometric analysis. These models should be reproducible and cost effective, and they should use species closest to humans. Whole blood is preferable to induce vasospasm, because erythrocyte hemolysate has been shown to be less capable of generating a delayed, sustained response (26,27). To induce vasospasm, a number of techniques have been used that lead to the development of delayed-onset, sustained arterial narrowing. These techniques can be grouped into 3 general categories: (i) puncture of an artery (endovascularly or under direct vision), (ii) surgical exposure of an artery and placement of an autologous blood clot obtained from another vessel, and (iii) injection of blood obtained from a peripheral vessel into the subarachnoid space. A disappointing feature common to all animal models of SAH and vasospasm is the lack of vasospasm-related ischemic, neurologic deficits (28), most likely secondary to an abundance of collateral blood flow in smaller vertebrates. However, in that most studies focus on the induction, prevention, and/or reversal of vessel constriction rather than on vasospasm-related ischemia, the absence of ischemic neurologic deficits in experimental animals has limited significance.

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